Target Validation

Validate a candidate target by holding your own experimental data up against the published record. Inflexa runs rigorous multi-method analysis on your omics, then assembles a tier-by-tier literature evidence chain (basic biology, preclinical, clinical) from targeted PubMed queries and public databases. The platform overlays the two: where your findings converge with the published record, where they contradict it, and where the translational chain has gaps that would derail an advancement decision.

What You Get

Deliverables

Evidence convergence map

A side-by-side view showing where your experimental findings align with published literature. Each convergence point links your differential expression or pathway result to a literature evidence claim, with the source papers, databases, and confidence scores that support it. Convergent signals between independent data sources are the strongest basis for target advancement decisions.

Literature:Inflammation 0.90TNFα/NF-κB NES 2.27CONVERGENT
Literature:Obesity 0.81IL2/STAT5 NES 1.89CONVERGENT
Literature:AP2M1 0.42conflicting evidenceCONFLICT

Contradiction report

Not all evidence agrees. The contradiction report surfaces findings where your results conflict with published literature or where the literature itself is divided. Each conflict is contextualized by species, model system, and disease stage, so you can assess whether the disagreement is meaningful or explained by experimental differences. For GLP1R, the platform identified conflicting evidence for AP2M1 (concordance 0.42) and coronary artery disease (concordance 0.33).

AP2M1Coronary Artery Disease100%50%0%50%100%42%33%58%67%SupportingContradicting

Translational gap analysis

A staged view of evidence across the translational chain: basic research, preclinical, and clinical. The analysis highlights where evidence is strong, where it thins out, and where gaps could derail a program. For GLP1R, evidence coverage is complete across all three stages, a strong signal for target maturity. For earlier-stage targets, this analysis identifies exactly where additional experiments are needed.

ClinicalPreclinicalBasic Research317404580
DECISION ENABLED

Advance or deprioritize targets based on convergent evidence from your data and the full published record. Targets with strong convergence across independent data sources and complete translational chains are the strongest advancement candidates.

Sample Output

GLP1R target validation: evidence integration

GLP1R: Indication Scores (Top 10)1,301 evidence items
Metabolic SyndromeWeight LossHeart FailureType 2 DiabetesObesityCoronary Artery DiseasePrediabetesInflammationSocial IsolationHypertension00.20.40.60.810.810.810.810.810.810.810.900.901.001.00
Evidence Convergence: Literature × Analysis3 convergent findings
Literature SignalAnalysis FindingCell ContextVerdict
Inflammation (0.90)TNFα/NF-κB NES 2.27IL-33 mast cellsConvergent
Obesity (0.81)IL2/STAT5 NES 1.89IL-4 eosinophilsConvergent
Type 2 Diabetes (0.81)Insulin secretion 0.70GLP1R pathwayConvergent
Contradiction Report2 conflicts detected
EntityConcordanceType
AP2M10.42Molecular interaction
Coronary Artery Disease0.33Disease association
Translational Evidence Chaincomplete coverage
Evidence items0100200300400500600Basic ResearchPreclinicalClinical580404317

CROSS-TARGET COMPARISON: EGFR (ONCOLOGY)

Dual-Target Evidence Profile: GLP1R vs EGFR2 targets compared
PapersEvidenceTrialsDrugsDiseases05001.0k1.5k2.0k2.5k2511.3k3173092861611.1k2.3k221148GLP1R (metabolic)EGFR (oncology)

EGFR has 7.2x more clinical trials (2,293 vs 317) reflecting oncology's trial-intensive development model. GLP1R has broader disease associations (286 vs 148) spanning metabolic, cardiovascular, and CNS indications.

EGFR: Top Indicationsall with clinical + human evidence
IndicationScoreEvidence Basis
NSCLC0.77clinical + human
GBM0.70clinical + human
CRC0.70clinical + human
EGFR: Modality Tractabilityall 4 modalities tractable
Small Molecule
TRACTABLE
Antibody
TRACTABLE
PROTAC
TRACTABLE
Other Clinical
TRACTABLE
Molecular PartnerInteraction Score
EGF0.97
STAT30.92
PTPN10.90
PTPN110.86
AP2M10.83
How It Works

Methodology

STEP 1

Assemble a literature evidence chain for the target

Inflexa runs targeted PubMed queries scoped to the target, then enriches with public sources (ChEMBL, Open Targets, ClinicalTrials.gov, FAERS, STRING). Each evidence claim carries a hyperlink to its supporting PMID or record. For GLP1R, this yielded 251 papers, 1,301 evidence items, and 317 clinical trials, organised into a basic-biology / preclinical / clinical chain.

STEP 2

Run differential expression

Inflexa analyzes your experimental omics data using DESeq2 with appropriate covariates. For the IL-4/IL-13/IL-33 dataset, this identified 4,272 differentially expressed genes across 62 samples in two cell types.

STEP 3

Pathway enrichment identifies biological processes

GSEA enrichment across Hallmark, KEGG, and Reactome gene sets identifies which biological processes are affected. The platform found TNFα/NF-κB signaling as the top IL-33 pathway (NES 2.27) and IL2/STAT5 as the top IL-4 pathway (NES 1.89).

STEP 4

Platform overlays results to find convergence

Literature disease associations are matched against experimental pathway and gene-level findings. Convergent signals (where independent evidence sources agree) are flagged as high-confidence. Contradictions are surfaced with concordance scores.

STEP 5

Translational gap analysis

Evidence is mapped across the translational chain (basic research → preclinical → clinical). Gaps at any stage are flagged. For GLP1R, the chain is complete with 580 basic research items, 404 preclinical items, and 317 clinical items.

Who This Is For

Target personas

Target biology lead

Assess whether experimental findings are consistent with the broader evidence base before committing to validation studies.

Translational science head

Identify translational gaps and contradictions that could derail programs, before they become expensive.

Portfolio reviewer

Compare targets by evidence maturity and convergence strength to allocate resources effectively.